Impacts of CO2 on acid-base balance, rectal base excretion and intestinal carbonate formation in marine fish

化石燃料的燃烧继续增加海洋二氧化碳(CO2)，导致海洋酸化。此外，富含二氧化碳的水在某些区域的周期性上升导致地表水严重酸化，这使得对升高的二氧化碳水平的检查在今天是有意义的。尽管海鱼很容易补偿在上升流地区观察到的二氧化碳水平和未来200年的预测水平，但人们对这些丰富的脊椎动物如何维持酸碱平衡(恒定的血液pH值)知之甚少。格罗塞尔和他的团队的初步发现表明，外部二氧化碳水平升高，低至750ppm二氧化碳，会导致海鱼的酸碱平衡失调，至少会产生部分补偿。格罗塞尔和他的团队正在研究海洋鱼类在外部二氧化碳升高的情况下保持酸碱平衡的机制。暴露在周围水中二氧化碳升高的后果是血液中二氧化碳的增加，而血液中碳酸氢盐(HCO3-)的快速增加平衡了这一结果，缓冲了酸中毒并维持了正常的PH值水平。早期的实验表明，血液中HCO3-的增加是通过增加从水中摄取HCO3-实现的，大概是通过鳃。格罗塞尔和他的团队的目标是确定参与这一过程的运输蛋白的分子性质。血液中的二氧化碳和HCO3-形成HCO3-通过肠道排泄的底物，这是鱼类维持盐分和水分平衡所必需的过程。PI和他的同事早期的研究已经证明了肠道组织血液侧的HCO3-水平与组织的HCO3-排泄率之间的关系。因此，在二氧化碳暴露期间，血液中HCO3-的升高可能会导致肠道组织排出更多的HCO3-，并导致血液中HCO3-的损失。Grosell和他的团队的最新发现证实了这一预期，计划中的研究将检查肠道HCO3运输系统在二氧化碳暴露期间是否调整，以促进血液HCO3-水平的保留。海水鱼肠道中的HCO3-与摄取的海水中的钙(Ca2+)结合，在肠腔中形成碳酸钙(CaCO3)，然后排出到环境中。认识到海洋鱼类以这种方式对海洋中CaCO3的形成有很大贡献是相对新颖的，这让Grosell和他的团队测试海洋二氧化碳的增加是否会导致海洋鱼类产生CaCO3的增加。作为该项目的一部分，将首次测定鱼产碳酸钙的溶解度。这些研究活动将包括对本科生、博士生和博士后研究员的培训，以及在人口结构高度多样化的社区开展的一些外展活动。

Combustion of fossil fuels continues to increase oceanic carbon dioxide (CO2) resulting in ocean acidification. In addition, periodic upwelling of CO2-rich water in certain zones results in significant acidification of surface waters, making examination of elevated CO2 levels relevant today. Although marine fish readily compensate for CO2 levels observed in upwelling regions and levels predicted for the next 200 years, relatively little is known about how these abundant vertebrates maintain acid-base balance (constant blood pH). Preliminary findings by Grosell and his team demonstrate that elevated external CO2 levels as low as 750 ppm CO2 induce an acid-base balance disturbance and at least partial compensation in marine fish. Grosell and his team are examining the mechanism by which marine fish maintain acid-base balance in the presence of elevated external CO2. A consequence of exposure to elevated CO2 in the surrounding water is an increase in blood CO2 that is balanced by a rapid increase in blood bicarbonate (HCO3-), buffering the acidosis and defending normal pH levels. Early experiments demonstrate that the increase in blood HCO3- is achieved by increased uptake of HCO3- from the water, presumably across the gills. Grosell and his team aim to identify the molecular nature of the transport proteins involved in this process. Blood CO2 and HCO3- form substrate for excretion of HCO3- by the intestine also, a process that is necessary for fish to maintain salt and water balance. Earlier studies by the PI and co-workers have demonstrated a relationship between HCO3- levels on the blood side of the intestinal tissue and the HCO3- excretion rates by the tissue. Thus, elevation of blood HCO3- during CO2 exposure will likely result in increased HCO3- excretion by the intestinal tissue and loss of blood HCO3-. The most recent findings by Grosell and his team confirmed this expectation and planned studies will examine if intestinal HCO3- transport systems adjust during CO2 exposure to facilitate retention of blood HCO3- levels. The HCO3- in the intestine of marine fish combines with the calcium (Ca2+) from ingested seawater to form calcium carbonate (CaCO3) in the intestinal lumen, which is subsequently excreted to the environment. The realization that marine fish, in this way, contribute substantially to the formation of CaCO3 in oceans is relatively novel and has lead Grosell and his team to test if elevated oceanic CO2 will result in increased CaCO3 production by marine fish. For the first time, the solubility of fish-produced CaCO3 will be determined as part of this project. These research activities will involve training of undergraduate students, PhD students, and a postdoctoral researcher, as well as a number of outreach activities in a community with highly diverse demography.